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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A population of 199 patients from Rochester, MN, was followed from the time of their first carotid or vertebral-basilar transient ischemic attack (TIA). Patients treated with anticoagulants had no significant difference in survival from untreated patients. Among patients with carotid TIA who received anticoagulants, the net probability of stroke was slightly but not significantly lower than in untreated patients. The difference favoring treated patients with vertebral-basilar TIA was significant starting at three months. The rate of intracranial hemorrhage was higher higher among all patients receiving anticoagulant treatment than among untreated patients and was significantly higher among those 55 to 74 years old. Almost all the hemorrhages occurred after a year or more of anticoagulant treatment and in patients more than 65 years old. Patients with high diastolic blood pressure had a significantly higher net probability of stroke than did patients with lower blood pressure and those receiving antihypertensive drugs. By implication, treatment of hypertension was effective in preventing stroke in patients with TIA. Linear discriminant analysis and actuarial analysis indicated that diastolic blood pressure and anticoagulant therapy were the only factors that influenced stroke occurrence. There was no suggestion that previous myocardial infarction, angina pectoris, valvular heart disease, cardiac arrhythmia, or congestive heart failure--individually or in combination--influenced the occurrence of stroke or survival.
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PMID:Carotid and vertebral-basilar transient ischemic attacks: effect of anticoagulants, hypertension, and cardiac disorders on survival and stroke occurrence--a population study. 65 61

Cardiac taurine levels are elevated in hypertension and congestive heart failure. A possible mechanism for this increase in taurine is an alteration of its uptake. We sought to identify and characterize a carrier-mediated transport system for taurine in the mammalian myocardium utilizing the fetal mouse heart in organ culture. Hearts from fetuses of 16-19 days gestational age used in these studies had an endogenous taurine content of 14.1+/-0.5 nmol/mg tissue. The uptake of [(3)H]taurine was linear for up to 8 h. Taurine was accumulated against a concentration gradient as demonstrated by a net increase in taurine concentration when hearts were incubated in 0.5 mM taurine. [(3)H]Taurine uptake was saturable, K(m) = 0.44 mM, temperature dependent, and required sodium. The close structural analogues, hypotaurine and beta-alanine, reduced [(3)H]taurine uptake by 87% when present in 100-fold excess. The alpha-amino acids alanine, alpha-aminoisobutyric acid, glycine, leucine, and threonine did not inhibit uptake. Other taurine analogues tested were guanidinotaurine, guanidinopropionic acid, gamma-aminobutyric acid, 2-aminoethane phosphonic acid, aminomethane sulfonic acid, 3-aminopropane sulfonic acid, N-acetyltaurine, and isethionic acid. We conclude that a carrier-mediated transport system for taurine exists in the fetal mouse heart based on the demonstration of (a) temperature dependence, (b) saturability, and (c) structural selectivity of the uptake process. Transport was demonstrated to be mediated by a beta-amino acid uptake system. In addition, taurine uptake was observed to be sodium dependent, energy dependent, and capable of accumulating taurine against a concentration gradient.
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PMID:Characterization of a carrier-mediated transport system for taurine in the fetal mouse heart in vitro. 65 83

Long-term follow-up of 137 patients who had an ascending aorta-right pulmonary artery anastomosis at the Children's Hospital of Philadelphia between 1966 and 1975 is presented. One hundred four patients survived the first hospitalization. Of the 81 patients currently alive, 30 have had a succesful corrective. operation. Nine patients died at the time of correction. Fifty patients have adequate pallation. Of the 56 deaths, only nine were shunt related. Late complications in the 104 first admission survivors included congestive heart failure (23%), pulmonary artery hypertension (7%), pulmonary vascular obstructive disease (1%), and shunt failure (9%). Special catheterization techniques to evaluate the shunt and its effect on the pulmonary arteries prior to surgical correction are described. The ascending aorta-right pulmonary artery anastomosis can provide effective palliation without interfering with subsequent corrective operations.
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PMID:Ascending aorta-right pulmonary artery anastomosis. Long-term results in 137 patients with cyanotic congenital heart disease. 66 59

A 20 year old woman with tetralogy of Fallot and an associated atrial septal defect presented with severe hypertension and congestive heart failure. She had been acyanotic for several years. An acute trial of antihypertensive therapy during cardiac catheterization resulted in severe systemic oxygen desaturation and loss of consciousness. Since surgical correction, antihypertensive therapy has been well tolerated. This case demonstrates the hemodynamic importance of systemic vascular resistance in tetralogy of Fallot and the need for extreme caution if aggressive antihypertensive therapy is attempted before surgical correction.
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PMID:Systemic hypertension complicating tetralogy of Fallot: effects of antihypertensive therapy. 68 43

A review of eight cases of myocardial rupture following myocardial infarction confirmed the association of rupture with advanced age, a preponderance of females, hypertension, and physical exercise after infarction. In four patients, electrocardiograms recording the events of rupture showed further S-T elevation, supraventricular tachycardia, and conduction defects. One case of septal rupture showed increase in the amplitude of the P waves. The combination of these changes with sudden reappearance of chest pain, development or worsening of congestive cardiac failure with hypotension, and the appearance of a precordial systolic murmur should aid in the earlier diagnosis of this complication which may be amenable to surgery. Successful repair of rupture has been reported during the acute phase of infarction and after variable periods of delay.
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PMID:Myocardial rupture in acute myocardial infarction: report of experience and review. 70 67

Serial study of 72-lead precordial ST-maps, SGOT, and SLDH was done in 30 cases of acute myocardial infarction. Infarct size was estimated by sum of ST elevation in all leads (sigma ST), number of sites showing ST elevation (NST), peak SGOT, and peak SLDH levels, and correlated with each other and with clinical features and hospital course. sigma ST correlated well with NST (r=0.92), but the correlations of sigma ST with SGOT (r=0.99) and SLDH (r=3.84) were better than those of NST with SGOT (r=0.22) and SLDH (r=0.53). There were close agreements between sigma ST and peak SGOT and peak SLDH except in the cases of non-transmural infarction, in whom smaller sigma ST suggesting small infract occurred with higher enzyme peaks indicating moderate or large infarct. Longer duration of chest pain, larger number of associated conditions (e.g. angina, hypertension, diabetes), complications (e.g. congestive heart failure, shock, arrhythmias) and mortality were associated with larger infarcts.
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PMID:Precordial ST-segment changes and serum enzyme levels in acute myocardial infarction. 73 32

Obesity leads to several complications that affect many body systems. This paper focuses mainly on the cardiovascular complications, which include coronary heart disease, cerebrovascular disease and stroke, and congestive heart failure; the last may be secondary not only to advanced coronary atherosclerosis, but also to other pathogenetic factors. The increased frequency of coronary heart disease in the obese is largely attributable to the commonly associated hypertension, diabetes mellitus and lipoprotein abnormalities, rather than the adiposity. The lipoprotein disorders that have a role in atherogenesis are decreased plasma concentrations of high-density lipoproteins and elevated plasma concentrations of low-density lipoproteins. Abnormalities in cholesterol metabolism are responsible for the increased frequency of cholelithiasis in obese persons. The factors that mediate the development of cardiovascular and gallbladder complications are correctable by an appropriate program of meal planning and physical activity.
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PMID:Medical complications of obesity. 73 18

An evaluation of the functional state of the left ventricle through an estimate of the mean Vcf (Vcf) and the ejection fraction (EF) was made i- 30 patients, subdivided into groups according to average blood pressure rate, degree of severity of the retinographic alterations and ECG pattern. In addition, the thickness of the interventricular septum (S), the posterior wall (PP) and the S/PP were measured. Lastly, the mass of the left ventricle was determined through the following formula: mass = (h1+h2+Dd)3 -- Dd3X1,050. Only one patient was under treatment with beta-blocking drugs, and no patient presented clinical symptoms of cardiac decompensation. The Vcf and the EF did not deteriorize when the hypertensive pattern worsened, while there was an expansion of the thickness of the S and an increase in the mass of the left ventricular. The increase of the ventricular mass, however, was not always found to be associated with normal functionality, nor was an increase of the mass always present even in cases of highly evident hypertension. It is likely, therefore, that other factors not taken into consideration (time factor, for example) play an important role in determining the functional state of the left ventricle and degree of hypertrophy.
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PMID:[An echocardiographic study of the anatomo-functional alterations of the left ventricle in patients with different degrees of systemic hypertension (author's transl)]. 75 79

The CO2 rebreathing method, a noninvasive indirect Fick procedure, has been previously validated in normal subjects at supine rest and during exercise. In the present study 29 nearly simultaneous measurements of cardiac output were made by CO2 rebreathing and dye dilution in 17 patients with cardiovascular disease, 11 with hypertension, and six with congestive heart failure. Cardiac output at supine rest averaged 5.52 +/- 0.31 L. per minute by CO2 and 5.62 +/- 0.32 L. per minute by dye dilution (r = 0.93). Successive cardiac output measurements by rebreathing varied 6.0 +/- 1.1 per cent (r = 0.96) and by dye dilution, 6.5 +/- 0.9 per cent. Changes in cardiac output during exercise or after beta-adrenergic blockade were reflected by the CO2 method. It is concluded that the CO2 method provides reliable measurements of cardiac output both at rest and during exercise in patients with hypertension or congestive heart failure. Further validation of the method is needed in various disease states before it can be widely applied.
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PMID:Validation of the CO2 rebreathing method for measuring cardiac output in patients with hypertension or heart failure. 78 59

Recently, the availability of a number of specific inhibitors of the renin-angiotensin system has made it possible to address certain critical questions concerning the role of angiotensin II in physiologic homeostasis and in a number of pathologic states. These studies indicate that angiotensin II does not have an obligatory role in blood pressure maintenance in the normal, sodium replete individual, but it is essential following sodium depletion. The role of angiotensin II in feedback control of renin secretion is confirmed as is its importance in aldosterone stimulation both in relation to posture and sodium depletion. Angiotensin II is responsible for the initial pressor response of experimental renovascular hypertension and appears to be important in the initiation of chronic renovascular hypertension. Converting enzyme blockers and competitive inhibitors of angiotensin II are helpful in the diagnosis of clinical renovascular hypertension and in the identification of renin dependent hypertensives. Homeostatic mechanisms leading to maintenance of blood pressure and accumulation of edema in experimental congestive heart failure appear to be dependent on angiotensin II.
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PMID:George C. Griffith lecture. The role of renin in normal and pathological cardiovascular homeostasis. 79 34


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